Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure

Abstract Pulmonary hypertension (PH) is a global health issue with a prevalence of 10% in ages >65 years. Right heart failure (RHF) is the main cause of death in PH. We have previously shown that monocrotaline (MCT)‐induced PH and RHF are due to an increase in oxidative stress. In this study, pro...

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Autores principales:	Firoozeh Farahmand, Akshi Malik, Anita Sharma, Ashim K. Bagchi, Pawan K. Singal
Formato:	article
Lenguaje:	EN
Publicado:	Wiley 2021
Materias:	antioxidants oxidative stress pulmonary hypertension right heart failure Physiology QP1-981
Acceso en línea:	https://doaj.org/article/9bf79c0b2a6a4b618641ed039ed9948c
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spelling	oai:doaj.org-article:9bf79c0b2a6a4b618641ed039ed9948c2021-11-27T15:48:30ZRole of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure2051-817X10.14814/phy2.15090https://doaj.org/article/9bf79c0b2a6a4b618641ed039ed9948c2021-11-01T00:00:00Zhttps://doi.org/10.14814/phy2.15090https://doaj.org/toc/2051-817XAbstract Pulmonary hypertension (PH) is a global health issue with a prevalence of 10% in ages >65 years. Right heart failure (RHF) is the main cause of death in PH. We have previously shown that monocrotaline (MCT)‐induced PH and RHF are due to an increase in oxidative stress. In this study, probucol (PROB), a strong antioxidant with a lipid‐lowering property, versus lovastatin (LOV), a strong lipid‐lowering drug with some antioxidant effects, were evaluated for their effects on the MCT‐induced RHF. Rats were treated (I.P.) with PROB (10 mg/kg ×12) or LOV (4 mg/kg ×12), daily 6 days before and 6 days after a single MCT injection (60 mg/kg). Serial echocardiography was performed and at 4‐week post‐MCT, lung wet‐to‐dry weight, hemodynamics, RV glutathione peroxidase (GSHPx), superoxide dismutase (SOD), catalase, lipid peroxidation, and myocardial as well as plasma lipids were examined. MCT increased RV systolic and diastolic pressures, wall thickness, RV end diastolic diameter, mortality, and decreased ejection fraction as well as pulmonary artery acceleration time. These changes were mitigated by PROB while LOV had no effect. Furthermore, PROB prevented lipid peroxidation, lowered lipids, and increased GSHPx and SOD in RV myocardium. LOV did decrease the lipids but had no effect on antioxidants and lipid peroxidation. A reduction in oxidative stress and not the lipid‐lowering effect of PROB may explain the prevention of MCT‐induced PH, RHF, and mortality. Thus targeting of oxidative stress as an adjuvant therapy is suggested.Firoozeh FarahmandAkshi MalikAnita SharmaAshim K. BagchiPawan K. SingalWileyarticleantioxidantsoxidative stresspulmonary hypertensionright heart failurePhysiologyQP1-981ENPhysiological Reports, Vol 9, Iss 22, Pp n/a-n/a (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	antioxidants oxidative stress pulmonary hypertension right heart failure Physiology QP1-981
spellingShingle	antioxidants oxidative stress pulmonary hypertension right heart failure Physiology QP1-981 Firoozeh Farahmand Akshi Malik Anita Sharma Ashim K. Bagchi Pawan K. Singal Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
description	Abstract Pulmonary hypertension (PH) is a global health issue with a prevalence of 10% in ages >65 years. Right heart failure (RHF) is the main cause of death in PH. We have previously shown that monocrotaline (MCT)‐induced PH and RHF are due to an increase in oxidative stress. In this study, probucol (PROB), a strong antioxidant with a lipid‐lowering property, versus lovastatin (LOV), a strong lipid‐lowering drug with some antioxidant effects, were evaluated for their effects on the MCT‐induced RHF. Rats were treated (I.P.) with PROB (10 mg/kg ×12) or LOV (4 mg/kg ×12), daily 6 days before and 6 days after a single MCT injection (60 mg/kg). Serial echocardiography was performed and at 4‐week post‐MCT, lung wet‐to‐dry weight, hemodynamics, RV glutathione peroxidase (GSHPx), superoxide dismutase (SOD), catalase, lipid peroxidation, and myocardial as well as plasma lipids were examined. MCT increased RV systolic and diastolic pressures, wall thickness, RV end diastolic diameter, mortality, and decreased ejection fraction as well as pulmonary artery acceleration time. These changes were mitigated by PROB while LOV had no effect. Furthermore, PROB prevented lipid peroxidation, lowered lipids, and increased GSHPx and SOD in RV myocardium. LOV did decrease the lipids but had no effect on antioxidants and lipid peroxidation. A reduction in oxidative stress and not the lipid‐lowering effect of PROB may explain the prevention of MCT‐induced PH, RHF, and mortality. Thus targeting of oxidative stress as an adjuvant therapy is suggested.
format	article
author	Firoozeh Farahmand Akshi Malik Anita Sharma Ashim K. Bagchi Pawan K. Singal
author_facet	Firoozeh Farahmand Akshi Malik Anita Sharma Ashim K. Bagchi Pawan K. Singal
author_sort	Firoozeh Farahmand
title	Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
title_short	Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
title_full	Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
title_fullStr	Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
title_full_unstemmed	Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
title_sort	role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure
publisher	Wiley
publishDate	2021
url	https://doaj.org/article/9bf79c0b2a6a4b618641ed039ed9948c
work_keys_str_mv	AT firoozehfarahmand roleofoxidativestressversuslipidsinmonocrotalineinducedpulmonaryhypertensionandrightheartfailure AT akshimalik roleofoxidativestressversuslipidsinmonocrotalineinducedpulmonaryhypertensionandrightheartfailure AT anitasharma roleofoxidativestressversuslipidsinmonocrotalineinducedpulmonaryhypertensionandrightheartfailure AT ashimkbagchi roleofoxidativestressversuslipidsinmonocrotalineinducedpulmonaryhypertensionandrightheartfailure AT pawanksingal roleofoxidativestressversuslipidsinmonocrotalineinducedpulmonaryhypertensionandrightheartfailure
_version_	1718408519721418752

Role of oxidative stress versus lipids in monocrotaline‐induced pulmonary hypertension and right heart failure

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